One form of cardiac arrhythmia with serious consequences is tachycardia. Tachycardia is a condition where an abnormally high heart rate severely affects the ability of the heart to pump blood. The higher the heart rate, the more dangerous the condition. In ventricular tachycardia (VT), the QRS complexes defining the heart rate are abnormally broad and occur at a rate in the range from about 100 to about 250 beats per minute. Sustained episodes of VT are particularly dangerous because they may deteriorate into ventricular fibrillation (VF), the most life-threatening cardiac arrhythmia. VF is the result of disordered, rapid stimulation of ventricular cardiac tissue, which prevents the ventricles from contracting in a coordinated fashion. VF may cause a severe drop in cardiac output and death if not quickly reverted.
Tachycardia is often the result of electrical feedback within the heart--a natural beat results in the feedback of an electrical stimulus which prematurely triggers another beat. Tachycardia control is frequently achieved by applying electrical stimulation to the heart. The application of electrical stimulation disrupts the stability of the feedback loop, thereby returning the heart to normal sinus rhythm.
One type of electrical stimulation therapy that is known for interrupting tachycardia is cardioversion shock therapy. Cardioversion shock therapy is performed by applying an electrical shock to cardiac tissue in order to depolarize the ventricular myocardium. This allows the site of fastest spontaneous discharge, typically the sinus node, to regain pacing control, thereby terminating the tachycardia episode. In known cardioversion systems, the cardioversion shock is electronically synchronized to fire at the R-wave following confirmation of the arrhythmia. Because of electronic delays which are the result of device switching and charging requirements, the shock is generally provided shortly after the confirming R-wave. Nevertheless, the shock is often administered while significant portions of cardiac tissue are still refractory from the confirming depolarization. A successful cardioversion shock that is administered while significant portions of cardiac tissue are refractory may require a higher energy content than would otherwise be the case. Also, an improperly timed cardioversion shock can cause an afterdepolarization which can prolong the arrhythmia and even lead to a lethal acceleration.
Another type of electrical stimulation therapy known for interrupting tachycardia is antitachycardia pacing. This type of therapy is typically provided by a pacemaker that delivers antitachycardia pacing pulses to cardiac tissue in a manner intended to revert the tachycardia episode. Antitachycardia pacing pulses are of much lower energy than cardioversion shocks, typically between about 25 .mu.joules and about 30 .mu.joules and accordingly, and such pacing pulses should be delivered when the heart is most responsive to external stimulation. More particularly, antitachycardia pacing pulses should be delivered when the heart is non-refractory.
Unfortunately, there is usually no way of knowing exactly when the refractory period associated with the preceding R-wave ends. In recent years, pacemakers that provide antitachycardia pacing therapy have employed various techniques in an attempt to deliver antitachycardia pacing pulses to the portion of the cardiac cycle most likely to lead to termination of the tachycardia episode. For example, U.S. Pat. No. 4,280,502 (Baker et al.) refers to a pacemaker which, after confirmation of a tachycardia episode, automatically initiates a search routine consisting of a sequence of stimulation pulses. The pulses are provided within a predetermined time interval after a confirmation tachycardia beat. The refractory period is estimated from the experimental results of the search routine, and the search is terminated when a normal heartbeat is detected. If the first search routine is unsuccessful at terminating the tachycardia episode, a second pulse is then applied following the previously determined refractory interval by a second interval which is also experimentally determined by a second search routine.
U.S. Pat. No. 4,390,021 (Spurrell et al.) refers to a pacemaker which generates a sequence of two electrical stimulation pulses to terminate tachycardia. The delay of the first stimulation pulse and the coupled delay between the first and the second pulse are each scanned through 16 discrete steps. Successful time delay parameters are permanently stored, and on the next confirmed episode of tachycardia, scanning begins with the most recent successful synchronization parameters.
U.S. Pat. No. 4,587,970 (Holley et al.) refers to a pacemaker which uses experimental data taken from a general sample population to determine a function estimating the relationship between refractory period and heart rate. A sequence of pacing pulses is generated at intervals defined by the predetermined function in an attempt to synchronize the pacing pulses to a time shortly after the end of the refractory period. If the tachycardia episode is not terminated, another sequence of pulses is generated. The rate of the new sequence is decreased or increased depending upon whether an unevoked heartbeat was sensed during the preceding sequence.
U.S. Pat. No. 4,398,536 (Nappholz et al.) refers to a programmable pacemaker which automatically increases the pulse rate. A burst of pulses is generated after the last heartbeat used to confirm tachycardia. The initial time interval between the last heartbeat used to confirm tachycardia and the first pulse in the sequence is equal to a measured heartbeat cycle less a fixed decrement. If tachycardia persists, another pulse burst is generated at a higher rate. After exceeding the maximum rate, the scanning resumes during the next cycle at the minimum rate. The last burst rate which is successful in terminating tachycardia is stored in the pacemaker and is used for the first burst generated following the next tachycardia confirmation.
The features described above have enabled pacemakers capable of providing antitachycardia pacing therapy to interrupt tachycardia. However, this technology is not applicable to implantable cardiac stimulating devices that provide cardioversion shock therapy. Indeed, the aforedescribed approaches taken with respect to antitachycardia pacing devices would be inappropriate for cardioversion shock therapy systems, because they require the generation and delivery of a "sequence" or "burst" of pulses. A sequence or burst of cardioversion shocks, which are typically several orders of magnitude greater in energy content than antitachycardia pacing pulses, would rapidly deplete limited energy reserves, and could possibly cause great discomfort to the patient.
Prior art cardioversion shock systems either provide no synchronization or they synchronize the stimulation pulses to fire immediately after an R-wave (that is, when the tissue is generally refractory), rather than in the period at which the heart is fully responsive to external stimulation (i.e., when the heart is in a repolarized state, or non-refractory state). During the refractory period of the heart, the cardiac muscle is insensitive to restimulation and cannot respond to a stimulus until after most of the repolarization process is completed.
Furthermore, the cardioversion shocks provided by some "synchronized" systems are administered at approximately the same time relative to the confirming R-wave regardless of the patient's heart rate. Since the timing of the repolarization period relative to the previous R-wave is a function of heart rate, these prior art systems that are heart rate independent do not accurately synchronize delivery of cardioversion shocks to the repolarization period. Consequently, these systems may administer shocks while the heart is generally refractory, may require higher than necessary energy content, and may require additional shocks, thereby increasing the possibility of discomfort to the patient and reducing the useful life of the implanted cardioverter.
What is needed, therefore, is an implantable cardiac stimulating device that attempts to administer a cardioversion shock during the period of the cardiac cycle when the heart is primarily repolarized, so that a lower energy cardioversion shock can effectively interrupt a tachycardia episode because the tissue is responsive to an electrical stimulation pulse. A cardioversion shock properly administered when the heart is responsive to an external stimulus, would optimize the chance of eliciting a heartbeat that preempts the next expected tachycardia beat.